Commit to an answer before revealing the explanation. Use the section menu to navigate; each question and answer has its own link. Five-option evidence updates ask for the most defensible direction of change; discuss a justified adjacent response.
Save and export your first responses
First choices and optional confidence stay in this browser and are not sent to the website. Opening an explanation first is recorded. Revisiting an unchanged case preserves the first response; revised cases receive a new version. Website visit analytics are separate. On a shared device, export and clear the history when finished.
Sections in this case
Question and answer links
- W1: An 88-year-old man who weighs 58 kg has a creatinine of 2.4 mg/dL at a routine visit; the laboratory reports an eGFR of · Answer
- W2: A patient with an eGFR of 25 asks which over-the-counter laxative is safest for long-term use. What do you recommend? · Answer
- Q3: Walter takes apixaban 5 mg twice daily for atrial fibrillation. He is 88, weighs 58 kg, and his creatinine four months a · Answer
- Q4: Walter's pressure is 126/68 seated and 104/60 standing at one minute, with lightheadedness, on amlodipine 10 mg daily; t · Answer
- Q5: At 11:20: potassium 6.1, magnesium 7.4, creatinine 2.9 (2.4 four months ago), bicarbonate 19, glucose 60 before the juic · Answer
- Q6: In the emergency department Walter's potassium is 6.0 with peaked T waves, his magnesium 7.3 with absent reflexes, pulse · Answer
- Q7: If you were thinking "progressive kidney failure requires starting dialysis during this admission," and you then learn t · Answer
- Q8: You ask yourself the surprise question — "Would I be surprised if Walter died in the next 12 months?" — and the honest a · Answer
Session S5 · 2026-11-03 · optional-30 · 30 min Anchor: Integrative review — geriatric and palliative nephrology basics · Integrates: eGFR interpretation in the elderly and drug dosing by kidney function (DOAC, sulfonylurea, TMP-SMX), trimethoprim hyperkalemia and the creatinine it raises without lowering GFR, hypermagnesemia from a laxative, frailty-adjusted blood pressure, outpatient triage of a potassium of 6.1, conservative kidney management and shared decision-making Runs 10:00–10:30 only if the full 150-minute block is available. One-line hook: An 88-year-old's patient portal says "Stage 4 kidney failure," and his son wants dialysis planned. The PA in the room has to decide which of today's numbers is the emergency, and what an eGFR can and cannot say at 88.
Fictional patient. Every name, date and number in this case is invented for teaching.
Learning Objectives
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
- Interpret a creatinine-based eGFR in a very old, low-muscle patient — its limits, the slope over years, and the drug that raises creatinine without lowering filtration.
- Dose or stop the common offenders by kidney function in an older adult — apixaban by the label's age, weight and creatinine rule, and magnesium laxatives — and name the deprescribing moves for sulfonylureas, NSAIDs and long-term PPIs (discussed, not tested).
- Triage a potassium of 6.1 with an ECG, and treat trimethoprim hyperkalemia and laxative hypermagnesemia — calcium first when the heart is involved.
- Individualize the blood-pressure target for frailty, using standing pressures.
- Distinguish a planning referral from a dialysis start, and offer conservative kidney management through a goals-of-care conversation.
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2
W1What an eGFR of 25 at 88 can and cannot say
An 88-year-old man who weighs 58 kg has a creatinine of 2.4 mg/dL at a routine visit; the laboratory reports an eGFR of 25 (CKD-EPI 2021). Which statement about that number is correct?
It is the creatinine clearance that drug labels use, so doses can be read straight off it
His low muscle mass lowers his creatinine, so the eGFR may overstate his true filtration
An eGFR in the 20s is normal aging at 88, so it is not chronic kidney disease
The equation subtracts so much for age that his true filtration is probably close to normal
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Low muscle mass can cause creatinine-based eGFR to overestimate filtration. When a decision depends on greater precision, consider cystatin C and a combined creatinine–cystatin C estimate, while remembering that cystatin C also has non-GFR determinants. Serial results establish trajectory; one eGFR cannot show progression. Why not the others: A — labels use Cockcroft–Gault creatinine clearance, which for him is about 17 mL/min, not 25; C — healthy aging costs about 0.75 mL/min a year , which takes no one to the 20s; D has the direction backwards. Course reading: Evidence for this case
W2The laxative for an eGFR of 25
A patient with an eGFR of 25 asks which over-the-counter laxative is safest for long-term use. What do you recommend?
Milk of magnesia (magnesium hydroxide) at bedtime
Magnesium citrate, one bottle whenever it is needed
Sodium phosphate, as an enema or by mouth
Polyethylene glycol (PEG 3350) powder in water
Show answer and explanation · Link to this question
Correct answer: D
Learning point: Healthy kidneys excrete extra magnesium so well that hypermagnesemia almost never happens with normal function; below an eGFR of 30, every magnesium laxative or antacid accumulates. Toxicity shows first as fading reflexes, then weakness, low blood pressure and slowed cardiac conduction. Polyethylene glycol holds water in the stool and adds no magnesium or phosphate; docusate and stimulant laxatives are the other alternatives. Why not the others: A and B are the products the hypermagnesemia lecture names for CKD stage 4–5; C — phosphate preparations are avoided below an eGFR of 30 because of the phosphate load. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q3 · Q4
Mr. Walter Kruse, 88, a retired dairy farmer, is brought to his primary-care clinic on a Monday morning by his son, Dennis, who runs the farm now. For a week Walter has been weak — "his legs won't hold him" — and constipated, and on Saturday he nearly fainted standing up from the kitchen table. Dennis has a second worry. On the patient portal his father's last result reads "eGFR 25 — Stage 4 kidney failure." "When does the dialysis start? Shouldn't we get it planned before his kidneys shut down?"
Walter has atrial fibrillation, type 2 diabetes for 25 years, hypertension, arthritis in both hips, and chronic kidney disease noted "for years." He walks with a cane, needs help to bathe, and fills his own pill box. Two weeks ago, more constipated than usual, he doubled his nightly milk of magnesia. Ten days ago an urgent care drained an abscess on his left forearm (culture: methicillin-resistant Staphylococcus aureus, MRSA) and started trimethoprim-sulfamethoxazole (TMP-SMX); nobody checked his kidney function at that visit. His wife died in an intensive-care unit after a long illness, and he has told Dennis more than once, "No machines for me."
Vitals (10:30): Temp 36.6 °C · Pulse 46, irregular · BP 126/68 seated → 104/60 standing at 1 minute, with lightheadedness (pulse 46 → 48) · Resp 14 · SpO₂ 95% on room air · Weight 58.0 kg (60.0 kg six weeks ago) · Height 175 cm.
Exam: Thin; slow to answer but oriented. Dry mucous membranes; neck veins flat; lungs clear. Irregularly irregular rhythm, no murmur. Abdomen soft, mildly distended. A healing 2-cm wound on the left forearm without surrounding redness. Hip-flexor strength 4/5. Biceps, knee and ankle reflexes absent (his chart from last spring records 1+ knee reflexes). No asterixis, no edema.
Medications
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Apixaban | 5 mg | PO | twice daily | Atrial fibrillation — stroke prevention |
| Glipizide | 5 mg | PO | twice daily | Type 2 diabetes |
| Amlodipine | 10 mg | PO | daily | Hypertension |
| Naproxen (over the counter) | 440 mg | PO | twice daily | Hip arthritis |
| Omeprazole | 20 mg | PO | daily — for 6 years | Stomach upset on naproxen |
| Milk of magnesia | 30 mL (2 tablespoons) | PO | nightly — doubled 2 weeks ago | Constipation |
| TMP-SMX double strength | 160/800 mg | PO | twice daily — started 10 days ago | MRSA forearm abscess |
Fingerstick glucose: 58 mg/dL. He drinks juice and eats crackers; 15 minutes later it is 96. His last hemoglobin A1c was 6.3%. Glipizide is stopped on the spot: sulfonylureas cause more hypoglycemia as kidney function falls, and the geriatric deprescribing list replaces them in frail older adults. A stat chemistry panel was drawn at 10:45, before the juice, and a 12-lead ECG is requested for the slow, irregular pulse; while you wait, you go through his medication list.
Pause — commit before the reveal
Q3The anticoagulant dose
Walter takes apixaban 5 mg twice daily for atrial fibrillation. He is 88, weighs 58 kg, and his creatinine four months ago was 2.4 mg/dL (eGFR 25; Cockcroft–Gault clearance about 17 mL/min). He has never had a stroke or a major bleed. Which change is correct?
Keep 5 mg twice daily; apixaban needs no change until the eGFR falls below 15
Stop the anticoagulant entirely; DOACs are contraindicated once the eGFR is below 30
Reduce to 2.5 mg twice daily; he meets the label's age, weight and creatinine rule
Switch to dabigatran 150 mg twice daily, which is better suited to weaker kidneys
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The apixaban label for atrial fibrillation lowers the dose to 2.5 mg twice daily when two of three are present — age 80 or older, weight 60 kg or less, creatinine 1.5 mg/dL or more (AF anticoagulation review §3.3) — and Walter meets all three. Dose by the label's own measure (here age, weight and creatinine; for other drugs, the renal metric specified by that product label), not by the eGFR on the portal. Whether to anticoagulate at all is a separate stroke-versus-bleeding decision. Why not the others: A ignores the age-weight-creatinine rule; B — apixaban remains usable at his eGFR with the label's dose; D — dabigatran is the DOAC most dependent on the kidney (about 80% renal) and is reduced or avoided below a clearance of 30. Course reading: Evidence for this case
Q4The standing pressure
Walter's pressure is 126/68 seated and 104/60 standing at one minute, with lightheadedness, on amlodipine 10 mg daily; two days ago he nearly fainted. He is 88, frail, diabetic, with CKD. What is the blood-pressure plan?
Reduce the amlodipine and set the dose by his standing pressure and symptoms
Keep amlodipine 10 mg, since his seated 126/68 already meets the CKD goal
Add lisinopril to push his seated systolic under 120, the target for CKD
Start midodrine for the orthostatic drop and continue the amlodipine 10 mg
Show answer and explanation · Link to this question
Correct answer: A
Learning point: A systolic fall of 22 mmHg on standing, with symptoms, is orthostatic hypotension (a fall of 20 systolic or 10 diastolic within 3 minutes ), and in a frail 88-year-old the falls it causes outweigh a few mmHg of seated pressure. Over 80 the target is individualized — according to frailty, symptoms, standing pressure and patient priorities — and symptomatic orthostasis calls for less medication, not another drug. Amlodipine is the one to cut (to 5 mg, or held while he is this dry), with standing pressures at every visit. Why not the others: B treats the seated number and ignores the near-faint; C applies a target meant for robust patients measured under standardized conditions to a man who cannot tolerate the pressure he has; D adds a drug to treat the side effect of another drug. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q5 · Q6 · Q7
Because his reflexes are gone and he takes a magnesium laxative, you add a magnesium level to the stat panel. Results return at 11:20; the 12-lead ECG is done in the exam room, and a bladder scan after he voids shows 60 mL.
| Test | Today (10:45) | 4 months ago | Reference range |
|---|---|---|---|
| Sodium | 137 | 139 | 135–145 mEq/L |
| Potassium | 6.1 | 4.9 | 3.5–5.0 mEq/L |
| Chloride | 108 | 106 | 98–107 mEq/L |
| Bicarbonate | 19 | 23 | 22–29 mEq/L |
| Anion gap (Na − [Cl + HCO₃]) | 10 | 10 | 8–12 mEq/L |
| BUN | 46 | 40 | 7–20 mg/dL |
| Creatinine | 2.9 | 2.4 | 0.7–1.3 mg/dL |
| eGFR (CKD-EPI 2021) | not valid — creatinine has moved | 25 | ≥60 mL/min/1.73 m² |
| Glucose (drawn before the juice) | 60 | 112 | 70–99 mg/dL |
| Calcium | 9.0 | 9.2 | 8.5–10.5 mg/dL |
| Magnesium | 7.4 | — | 1.7–2.2 mg/dL |
| Phosphorus | 4.4 | 4.1 | 2.5–4.5 mg/dL |
| Albumin | 3.5 | 3.7 | 3.5–5.0 g/dL |
| Hemoglobin | 11.2 | 11.5 | 13.5–17.5 g/dL |
| Urine albumin-to-creatinine ratio | — | 280 | <30 mg/g |
| Urinalysis | SG 1.012; protein 1+; blood, leukocyte esterase and nitrite negative; no cells or casts | — | — |
12-lead ECG: atrial fibrillation, ventricular rate 46; QRS 0.09 s (narrow); tall, peaked T waves in V2–V4.
Anion gap 137 − (108 + 19) = 10, and 11 after correcting for an albumin of 3.5: a mild normal-gap acidosis has appeared alongside the high potassium. BUN:creatinine 16:1. The creatinine is 0.5 mg/dL above his value of four months ago — 1.2 times baseline.
Pause — commit before the reveal
Q5Today, or in 48 hours?
At 11:20: potassium 6.1, magnesium 7.4, creatinine 2.9 (2.4 four months ago), bicarbonate 19, glucose 60 before the juice. The ECG shows atrial fibrillation at 46 with peaked T waves. He is weak, his reflexes are absent, he nearly fainted two days ago, and the bladder scan shows 60 mL. What is the disposition?
Stop TMP-SMX and milk of magnesia; repeat the panel in clinic in 48–72 hours
Give a potassium binder in the clinic, stop TMP-SMX, and recheck the potassium tomorrow
Admit him directly to the hospital for a dialysis catheter and urgent hemodialysis tonight
Send him by monitored ambulance to the emergency department now, with the ECG
Show answer and explanation · Link to this question
Correct answer: D
Learning point: An unexpected creatinine rise in clinic gets the same moves every time — repeat the chemistry, review drugs and intake, look at the urine, scan the bladder — then a choice between same-day care and a 48–72-hour recheck, made from the potassium, the ECG, the symptoms and the trajectory. Here a potassium of 6.1 comes with ECG changes and a rate of 46, the magnesium has taken his reflexes, and he was hypoglycemic an hour ago: each needs monitored treatment today . The clinic stops the culprits and hands him on. Why not the others: A triages by the creatinine and misses the ECG; B — a binder lowers potassium over hours and does nothing for the heart or the magnesium; C reaches for dialysis before calcium, a shift and his own kidneys have had a chance. Course reading: Evidence for this case
Forty minutes later, in the emergency department: potassium 6.0, magnesium 7.3, pulse 46, BP 108/62 lying down, glucose 96; the ECG is unchanged.
Q6First in the emergency department
In the emergency department Walter's potassium is 6.0 with peaked T waves, his magnesium 7.3 with absent reflexes, pulse 46, BP 108/62 lying down, glucose 96 after juice. Which treatment comes first?
Intravenous calcium gluconate to steady the heart against the potassium and the magnesium
Regular insulin 10 units intravenously on its own, so the potassium falls within 15 minutes
A dialysis catheter and urgent hemodialysis to remove the potassium and the magnesium together
A sodium polystyrene sulfonate enema to pull the potassium out through the colon first
Show answer and explanation · Link to this question
Correct answer: A
Learning point: IV calcium treats the hyperkalemic ECG changes and antagonizes magnesium's cardiac and neuromuscular effects. It lowers neither concentration. In parallel, stop the sources, use insulin with dextrose under close glucose surveillance to shift potassium, and arrange elimination. Correct volume depletion and use a loop only when urine output and volume assessment support it. Early nephrology review is appropriate for symptomatic hypermagnesemia with impaired renal clearance; refractory toxicity may need dialysis. Why not the others: B — insulin without dextrose, an hour after hypoglycemia, invites a second low and does nothing for the magnesium; C trades minutes for hours; D — sodium polystyrene is slow and risks colonic injury in a constipated man. Course reading: Evidence for this case
The emergency team gives calcium gluconate, then a liter of isotonic saline followed by furosemide, sodium zirconium cyclosilicate (a potassium binder), and dextrose with a small insulin dose, checking glucose at baseline, every 30 minutes for 2 hours, then hourly through at least 6 hours, with longer surveillance after recurrent hypoglycemia. TMP-SMX, milk of magnesia and naproxen are stopped (glipizide already was); amlodipine is held. Six hours later: potassium 5.2, magnesium 5.6. By morning: potassium 4.7, magnesium 3.9, knee reflexes back, ventricular rate in the 70s, glucose 110–150 without glipizide. The surgeon checks the forearm — drained, ten days of treatment, healing — and no further antibiotic is needed.
On rounds Dennis stops the hospitalist in the hall: "His creatinine was 2.9 — the worst it's ever been. Is this the kidney failure starting? Should we be planning dialysis now?" The hospitalist pulls three years of clinic results.
Q7Evidence update
Concordance-style practice: there is no expert panel behind this key, the teaching explanation. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."
If you were thinking "progressive kidney failure requires starting dialysis during this admission," and you then learn that his six clinic values over the past 36 months ran between an eGFR of 24 and 28 (creatinine 2.2–2.5) before this illness, that apart from what the magnesium explained he has had no nausea, itching or confusion, and that his 2-year KFRE is 8% (5-year, 23%), this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: B
Formative evidence update: The letter is a teaching anchor. Accept a justified adjacent response; this is not an expert-panel-validated score. Learning point: The serial results show little progression, and the creatinine change followed trimethoprim exposure, which can inhibit creatinine secretion. True AKI still requires assessment; the drug effect cannot be assumed to explain every rise. Symptoms improve as the acute electrolyte and drug problems are treated, so there is no demonstrated need to start dialysis during this admission. His CKD still warrants follow-up and goals-based planning. Either A or B can be justified; the learning target is the reduced likelihood of an immediate dialysis indication, not a validated distinction between the two labels. Why not the others: A treats a slow slope as no disease, when his G4 CKD still earns a planning conversation; C ignores three years of data; D and E read the 2.9 as progression without noticing the drug that started ten days before it. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q8
Three weeks later, back in clinic: potassium 4.6, magnesium 2.3, creatinine 2.4 (eGFR 25 — back on his line), home glucose readings 104–160 without glipizide, and a blood pressure of 138/74 seated and 130/70 standing on amlodipine 5 mg, with no lightheadedness. Acetaminophen and a topical diclofenac gel have replaced the naproxen, polyethylene glycol has replaced the milk of magnesia, omeprazole is stepping down to every other day on its way off, and apixaban is 2.5 mg twice daily.
Dennis has his question ready: "So what's the plan for when his kidneys do fail?" Walter answers first. "I've told you. No machines. I want to be on the farm with the dog."
Pause — commit before the reveal
Q8What to do with "no"
You ask yourself the surprise question — "Would I be surprised if Walter died in the next 12 months?" — and the honest answer is no: he is 88, frail, and has just survived a dangerous admission. He has said "no machines" for years; Dennis wants dialysis planned. What do you do with that answer?
Tell them dialysis is not an option at his age, and close the conversation
Refer him to hospice now, because a "no" to the surprise question means hospice
Hold a goals-of-care conversation with both and offer active conservative care
Order vein mapping and a fistula consult so an access is ready if needed
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The surprise question is a screen the clinician asks privately; a "no" is a reason to talk, not a verdict. Ask Walter what he understands, fears and values most, recommend a plan that fits, and write it down. Conservative kidney management is that plan as active care — symptoms, potassium, acidosis, anemia and fluid still managed, palliative support when needed — and a planning referral at an eGFR under 30 fits inside it, because a referral is not a dialysis start. Why not the others: A decides by age instead of by the patient; B confuses a prognostic screen with a hospice referral; D prepares for a treatment he has refused, on a slope that may never need it. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
Two weeks later Walter, Dennis and the nephrology nurse practitioner spent an hour together. The plan they signed: no dialysis; keep treating what can be treated; potassium, magnesium and creatinine every three months; a do-not-resuscitate order Walter asked for himself; a call to the clinic for weakness, confusion or a fall. Dennis said afterward that he had been asking for a plan, not for a machine. Four drugs are gone — naproxen, glipizide, milk of magnesia and TMP-SMX — and a fifth, omeprazole, is tapering off; apixaban is 2.5 mg twice daily and amlodipine 5 mg, with acetaminophen and topical diclofenac for his hips and polyethylene glycol for constipation. A year later his eGFR is 24.
Clinical Pearl — At 88, an eGFR is a slope, not a stage Low muscle mass may make creatinine-based eGFR overestimate filtration. Review serial values and consider a combined creatinine–cystatin C estimate when precision matters. KFRE estimates treated kidney-failure risk; it does not replace assessment of frailty, competing mortality, symptoms or patient preference.
Clinical Pearl — Trimethoprim: two effects, one drug It blocks the collecting duct's sodium channel (ENaC) the way amiloride does, so potassium rises with a mild normal-gap acidosis — type 4 RTA physiology — and it blocks the tubule's secretion of creatinine, raising creatinine 0.2–0.5 mg/dL without lowering GFR . The potassium is the dangerous half: check potassium and creatinine soon after starting it in anyone with CKD.
Clinical Pearl — Magnesium out, polyethylene glycol in Milk of magnesia and magnesium citrate accumulate below an eGFR of 30. Reflexes disappear first (above about 7 mg/dL), then come weakness, low blood pressure and slowed conduction. IV calcium antagonizes magnesium within minutes; stopping the source and helping the kidney excrete it do the rest.
Clinical Pearl — Dose by the label's own measure For atrial fibrillation, apixaban is reduced to 2.5 mg twice daily when at least two label criteria are met: age at least 80, weight at most 60 kg and creatinine at least 1.5 mg/dL. Other drugs may use different renal measures; follow their labels. Review sulfonylureas after hypoglycemia, avoid nephrotoxic self-medication and deprescribe a PPI only after checking its indication.
Pitfall — "Stage 4" means dialysis A planning referral is not a dialysis start, and a very old patient with a flat slope may never need one. The question to answer is what the patient wants, not what the portal says.
Pitfall — Insulin without dextrose in a hypoglycemia-prone patient Shifting potassium with insulin in someone on a sulfonylurea with low kidney function invites a second, delayed low. Give dextrose with it and check glucose every hour .
Concept Links
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.
Concepts: aki-27, ckd-04, ckd-18, ckd-21, ckd-22, ckd-24, ckd-25, htn-cardiorenal-04, lytes-13, lytes-14, lytes-18, structural-18, structural-25, structural-26.
Source verification — 2026-10-12
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
Observational evidence in older sulfonylurea users (PMID 24858839) associates co-trimoxazole with increased severe hypoglycemia risk; monitor glucose and reconsider the combination, especially during reduced intake and kidney dysfunction.
US TMP-SMX labeling gives the usual regimen above CrCl 30 mL/min, half the usual regimen at 15–30, and use not recommended below 15. The infection, potassium, glucose and drug interactions still determine whether this is the appropriate antibiotic; a renal adjustment does not remove this patient’s adverse effects.